We wish to determine whether a specific increase in the responsiveness of the renal vasculature to angiotensin II occurs in rabbits with 1- and 2-kidney Goldblatt hypertension, and if so whether a lessened ability to synthesize renal prostaglandin E (PGE) may account for greater angiotensin responsiveness. This phenomenon will be studied in vivo in the normally perfused kidney in which blood flow is measured and in the kidney perfused wtih a pump in which perfusion pressure is monitored. The renal influence of PGE or a PG-like substance in the systemic circulation as well as that locally formed in the kidney will be evaluated in rabbits with 1- and 2-kidney Goldblatt hypertension and altered salt intake. A PG synthesis inhibitor will be administered i.v. and intraarterially to the kidney and its effect determined on renal blood flow, the renal AV difference of PGE and the 13,14-dihydro 15-keto metabolite of PGE. Further studies will be carried out to ascertain how renin from the ischemic kidney affects vascular resistance, PGE and renin release in the contralateral kidney in the dog. The modulating effect of PGE on the contralateral kidney will be studied by administering a PG synthesis inhibitor. The last part of this proposal will involve comparing renal adrenergic transmitter release in normal and 2-kidney Goldblatt hypertensive rabbits and determining whether angiotensin II is responsible for augmented transmitter release in the hypertensives.